Intestinal Metaplasia of the Bladder I ntestinal metaplasia of the bladder, or cystitis glandularis of the intestinal type (CGIT), is defined by the presence of intestinal type epithelium in the bladder. CGIT may be focal or diffuse; it is thought to be reactive process in response to urothelial injury such as chronic infection or irritation, as seen in patients with a neurogenic bladder, long-standing stone disease or long-term catheterization. Pa- tients typically present with voiding complaints such as hematuria, muscosuria, dysuria, urgency or obstructive symptoms. Although CGIT may be confined to surface epithelium, it more typically involves the underlying lamina propria. It has a predilec- tion for the bladder neck and trigone. Grossly, the lesion may be flat and inconspicuous, or it may be a readily evident mucosal abnor- mality, with prominent edema and inflammation. Infrequently, an exuberant proliferation results in a nodule or a papillary or polypoid lesion, suspicious for malignancy (fig. 1). Occasionally a mass may be evident on computerized tomography or ultrasound. Histologically, intestinal metaplasia is characterized by glands lined by mucin producing tall columnar epithelial cells, including occasional globet cells, not surrounded by transitional cells as is often the case in typical cystitis glandularis (fig. 2). In short, the findings resemble intestinal epithelium to the extent that other intestinal cell types (Paneth cells, argentaffin cells and argyrophilic cells) have been described in this condition, and even the histochem- ical staining properties of CGIT are similar to those of intestinal epithelium. 1 The extent of mucin production is variable. Mucin is occasionally extravasated into the stroma, a finding that is noted in some cases of endocervicosis of the bladder, but more importantly raises con- cern for a diagnosis of mucin-producing adenocarcinoma. With CGIT there is a generally orderly distribution of glands that are usually confined to the lamina propria, although minimal involve- ment of superficial muscularis propria has been described, whereas adenocarcinoma is characterized by cytologic atypia and randomly distributed glands that may infiltrate any level of the bladder wall. The absence of cytologically atypical cells either floating in pools of mucin or at the periphery of the mucin pools supports a benign diagnosis (fig. 2). Endocervicosis, in contrast to CGIT, is much more likely to involve the muscularis propria, and the mucin extravasa- tion in this condition incites an inflammatory and fibroblastic stro- mal response, a finding not typically associated with mucin extravasation from CGIT. 1 Sporadic reports describing the occurrence of adenocarcinoma in a background of long-standing CGIT have led to speculation that CGIT is a premalignant lesion. However, no instances of bladder adenocarcinoma were identified in 50 patients with CGIT followed for more than 10 years, suggesting that CGIT is not a strong risk factor for cancer. 2 Typically, suspicious lesions are biopsied or re- sected locally, and treatment is directed at the source of irritation and/or inflammation, such as stones or persistent infection. Bradley D. Figler, Jack S. Elder and Gregory T. MacLennan Departments of Pathology and Urology University Hospitals of Cleveland Case Western Reserve University Cleveland, Ohio REFERENCES 1. Young, R. H. and Bostwick, B. G.: Florid cystitis glandularis of intestinal type with mucin extravasation: a mimic of adeno- carcinoma. Am J Surg Pathol, 20: 1462, 1996 2. Corica, F. A., Husmann, D. A., Churchill, B. M., Young, R. H., Pacelli, A., Lopez-Beltran, A. et al; Intestinal metaplasia is not a strong risk factor for bladder cancer: study of 53 cases with long-term follow-up. Urology, 50: 427, 1997 FIG. 1. Inflamed edematous bladder mucosa involved by intestinal metaplasia, forming clinically worrisome polypoid lesion. FIG. 2. Intestinal metaplasia with extravasated mucin in stroma. No atypical cells are present within or at periphery of mucin lakes, confirming benign lesion. Pathology Page 0022-5347/06/1753-1119/0 Vol. 175, 1119, March 2006 THE JOURNAL OF UROLOGY ® Printed in U.S.A. Copyright © 2006 by AMERICAN UROLOGICAL ASSOCIATION DOI:10.1016/S0022-5347(05)00766-4 1119